神经病理性疼痛（neuropathic pain, NP）的既往研究中关于Homer1蛋白和Ⅰ组代谢型谷氨酸受体（metabotropic glutamate receptor, mGluRs）在疼痛信号转导中的作用相对明确，但它们相互之间的关系并不清楚，在突触后膜中Homer1蛋白和Ⅰ组mGluRs可以相互作用并对疼痛信号转导和疼痛维持有重要影响，Homer1蛋白可能是其中的关键靶点。Homer1b/c作为重要的突触后致密物在突触可塑性调节和突触信号传递中起重要作用。文章综述了Homer1蛋白特殊的果蝇激活蛋白/血管舒张刺激磷酸蛋白同源结构域1（enabled protein of drosophila/vasodilator‑stimulated phosphoprotein homology, EVH1）和螺旋卷曲（coiled‑coil, C‑C）结构在脊髓突触后膜通过与不同突触后蛋白结合产生NP作用，mGluRs在神经损伤模型的潜在作用机制中与上述作用可能存在共同的作用机制。
For neuropathic pain (NP), previous studies have demonstrated the role of Homer1 protein and groupⅠ metabotropic glutamate receptors (mGluRs) in pain signaling transduction, but their relationship is not clear. The Homer1 protein and groupⅠmGluRs in the posterior membrane can interact with each other, with great impact on pain signaling transduction and pain maintenance. Homer 1 protein may act as a key target. Homer1b/c as an important post‑synaptic dense substance is crucial in synaptic plasticity regulation and synaptic signaling transduction. This paper reviews a specific enabled protein of drosophila/vasodilator‑stimulated phosphoprotein homology (EVH1) and coiled‑coil (C‑C) structures of Homer1 protein in the spinal cord postsynaptic membrane to produce neuropathic pain through binding to different postsynaptic proteins, and a possible co‑action mechanism of metabolic glutamate receptor may exist in the potential mechanism of nerve injury model.
Cited
)
